Impaired endothelium-dependent relaxation of human hepatic arteries after preservation with the University of Wisconsin solution

Objective: To evaluate the effect of University of Wisconsin solution on endothelium-dependent relaxation and contraction of human hepatic arteries in vitro. Designs Human hepatic arteries were harvested from 24 patients with hepatocellular carcinoma who had undergone hepatectomy. Setting: A tertiary care center. Interventions: Human hepatic arteries (n=6 in each group) were harvested during resection for hepatocellular carcinoma. The arteries in group 1 (ie, the control group) were immediately studied without preservation. The arteries in group 2 were preserved in cold (4°C) physiological solution for 1 hour, while the arteries in groups 3 and 4 were preserved in University of Wisconsin solution for 1 and 16 hours, respectively. Segments of control and preserved hepatic arteries with or without endothelium were then suspended in organ chambers to measure the isometric force. Results: The relaxation of segments of the hepatic arteries with endothelium in response to acetylcholine and adenosine diphosphate was significantly (P<.05) greater than that of segments without endothelium. The maximal relaxation of hepatic arterial segments with endothelium in groups 3 and 4 in response to acetylcholine was notably different from that of segments in groups 1 and 2. The maximal relaxation of hepatic arterial segments with endothelium in groups 3 and 4 in response to adenosine diphosphate was notably different from that of segments in groups 1 and 2. Perfusate hypoxia (mean±SD PO₂, 30±5 mm Hg) caused the endothelium- dependent contraction of the arteries (the median initial tension in groups 1, 2, 3, and 4 was 251%, 233%, 276%, and 260%, respectively; P>.05). Conclusions: The endothelium-dependent relaxation of human hepatic arteries in response to acetylcholine and adenosine diphosphate was notably attenuated by University of Wisconsin solution. The impaired endothelium- dependent relaxation by University of Wisconsin solution and the prominent endothelium-dependent contraction of human hepatic arteries would favor vasospasm and thrombosis after hepatic transplantation.